Why the study?
The role of small conductance Ca2+-dependent potassium channels in the pathogenesis of diabetic cardiomyopathy remains uncertain.
SK channels appear to have increased activity or expression in epicardial cardiomyocytes of diabetic rats, contributing to altered action potential repolarization.
SK channel findings in diabetic rat hearts are hypothesis-generating; leaves open any role in human diabetic cardiomyopathy.
The role of small conductance (SK) Ca2+-dependent potassium channels in pathogenesis of diabetic cardiomyopathy remains uncertain. In our studies in the rat model of streptozotocin-induced type 1 diabetess mellitus (STZ-DM1) a significant increase above control in the prevalence of extracellular action potentials (eAP) recorded from isolated heart left ventricles and terminating with a prominent phase of after-hyperpolarization was observed. In experiments with local delivery to the site of recording of several tested potasssium channel blockers suppression of this phase of eAP after hyperpolarization was achieved only with application of apamin, the selective SK channel inhibitor. These data suggest that eAP afterhyperpolarization phase is associated with activation of SK channels and that activity and/or expression of these channels is increased in epicardial cardiomyocytes of left ventricles of STZ-DM1 rat hearts.
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Кубасов et al. (2021) studied this question.
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